In Drosophila, chromosome ends are maintained by the targeted transposition of two retrotransposons, HeT-A and TART. In the wild type, the frequency of transposition is sufficient to balance the gradual shortening of chromosome ends due to incomplete DAN replication. Mutations are known that drastically increase or decrease the frequency of HeT-A addition to a chromosome end, suggesting that this process in under genetic control. We have characterized one such mutation, and we are using positional information to clone the gene. A w+ transgene inserted into the telomere associated sequence (TAS) immediately proximal to the terminal HeT-A/TART array is repressed and variegates. This variegation appears to be due to an interaction of repression induced by TAS and activation initiated by HeT-A. The w+ transgene provides an assay for HeT-A transcription. Thus, these transgenes may provide a means to investigate mechanisms of HeT-A transcription and transpostion, and telomere elongation. We have found that w+ activity varies with changes in TAS sequences on the homologous telomere, as well as at other telomeres. Defects in, or deletions of, one of these TAS arrays increase w+ activity, and by extension HeT-A transcription. This may provide a means to increase transposition when one or more telomeres become short. To investigate the mechanism of HeT-A activation, we have collected radiation-induced mutations and insertional mutations that affect w+ activity. While these mutations affect w+ activity on several different telomeres, they have no effect on gene silencing at non-telomeric positions. Analysis of these mutations is ongoing. Mapping experiments indicate that all of the mutations on chromosome 2 reside at or near the left telomere. Many of these mutations are homozygous lethal and fail to complement mutations in the gene that is immediately adjacent to the telomere at 2L.